This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Teramoto, S. Articles by Ishii, M. Search for Related Content PubMed PubMed Citation Articles by Teramoto, S. Articles by Ishii, M.

Aging, the Aging Lung, and Senile Emphysema Are Different

In his recent editorial, Tuder implicated the pathophysiologic interrelationship between aging and cigarette smoke in the development of chronic obstructive pulmonary disease (COPD) (1). We believe that some of the points in this editorial are misleading.

First, aging is a process leading to death and is characterized by universal progressive, deleterious, and irreversible alterations. But aging is not a disease. We can treat the age-related phenomena, but not aging itself. Tuder is commenting on the article by Sato and coworkers in the same issue, which is entitled "Senescence Marker Protein-30 Protects Mice Lungs from Oxidative Stress, Aging, and Smoking" (2). Sato and coworkers' title is incorrect. Importantly, previous studies have described physiologic changes of the lungs due to aging alone as aging lung or senile lung, but not as senile emphysema (3, 4). Here, the lungs were characterized as undergoing airspace enlargement without alveolar wall destruction (3, 4). Also, Janssens and coworkers' review, which was cited by Tuder, did not correctly differentiate the difference between aging lung and senile emphysema (5). Thus, age itself is known to be a risk for COPD, but not necessary for the development of COPD.

Second, gene regulation of aging is complex. The master gene of aging has not been determined, although the Klotho gene is a candidate (6). Klotho gene–deficient mice develop the airspace enlargement without cigarette smoke exposure. Although mouse models of COPD often exhibited homogeneous alterations of lung structures, age-related changes of the lungs are heterogeneous in humans. The role of a single gene on the functional and morphologic changes of the lungs may be limited in humans. The redundancy of multiple genes associated with aging may substitute for the impaired cell function of lungs in humans due to a single gene defect.

Third, there is no association of apoptosis and aging in human lungs. In particular, apoptotic cell death is not directly related to the aging process. Because apoptosis is an active process, it is not related to a degenerative process such as aging.

We realized that the senescence marker protein-30 (SMP-30) gene is a good candidate gene for exploring the aging process and age-related diseases. However, the pathologic interaction between the aging process and COPD may not be solved by analyzing the SMP-30 gene and its protein products. We should differentiate physiologic aging, such as the aging/senile lung, from pathologic aging, as in senile emphysema (4). Furthermore, the resemblances and differences between senile emphysema and adult COPD should be better clarified.

Shinji Teramoto and Masaki Ishii

University of Tokyo, Tokyo, Japan

FOOTNOTES

Conflict of Interest Statement: Neither author has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

REFERENCES

1. Tuder RM. Aging and cigarette smoke: fueling the fire. Am J Respir Crit Care Med 2006;174:490–491.[Free Full Text]
2. Sato T, Seyama K, Sato Y, Mori H, Souma S, Akiyoshi T, Kodama Y, Mori T, Goto S, Takahashi K, et al. Senescence marker protein-30 protects mice lungs from oxidative stress, aging, and smoking. Am J Respir Crit Care Med 2006;174:530–537.[Abstract/Free Full Text]
3. Teramoto S, Fukuchi Y, Uejima Y, Teramoto K, Oka T, Orimo H. A novel model of senile lung: senescence-accelerated mouse (SAM). Am J Respir Crit Care Med 1994;150:238–244.[Abstract]
4. Teramoto S. Age-related changes in lung structure and function in the senescence-accelerated mouse (SAM): SAM-P/1 as a new model of senile hyperinflation of lung. Am J Respir Crit Care Med 1997;156:1361.[Medline]
5. Janssens JP, Pache JC, Nicod LP. Physiological changes in respiratory function associated with ageing. Eur Respir J 1999;13:197–205.[Abstract]
6. Kuro-o M, Matsumura Y, Aizawa H, Kawaguchi H, Suga T, Utsugi T, Ohyama Y, Kurabayashi M, Kaname T, Kume E, et al. Mutation of the mouse Klotho gene leads to a syndrome resembling ageing. Nature 1997;390:45–51.[CrossRef][Medline]

This article has been cited by other articles:

				H. Fehrenbach Animal models of pulmonary emphysema: a stereologist's perspective Eur. Respir. Rev., December 1, 2006; 15(101): 136 - 147. [Abstract] [Full Text] [PDF]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Teramoto, S. Articles by Ishii, M. Search for Related Content PubMed PubMed Citation Articles by Teramoto, S. Articles by Ishii, M.